May 2003
Volume 44, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2003
A Prolongation of Retinal Ganglion Cell Proliferation and Differentiation in MEK1(E) Transgenic Mice
Author Affiliations & Notes
  • H. Liu
    Department of Cell Biology, The Scripps Research Institute, La Jolla, CA, United States
  • X. Gong
    Department of Cell Biology, The Scripps Research Institute, La Jolla, CA, United States
  • Footnotes
    Commercial Relationships  H. Liu, None; X. Gong, None.
  • Footnotes
    Support  NIH Grant RO1EY12808 and RO1EY13849
Investigative Ophthalmology & Visual Science May 2003, Vol.44, 117. doi:
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      H. Liu, X. Gong; A Prolongation of Retinal Ganglion Cell Proliferation and Differentiation in MEK1(E) Transgenic Mice . Invest. Ophthalmol. Vis. Sci. 2003;44(13):117.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract

Abstract: : Purpose: To investigate molecular mechanisms for how retinal cells compensate for the enlarged eyeball of transgenic mice that express an active form of the mitogen-activated protein kinase kinase1 (MEK1) in the lens. Methods: BrdU labeling was used for monitoring cell proliferation in the retina. Both transgenic mice and wild type littermates, at ages of 2,3,4, 5 and 6 weeks, were intraperitoneally injected with BrdU. The eyes of the BrdU injected mice were harvested, sectioned and stained with anti-BrdU antibody, anti-neuronal nuclei NeuN (a marker for neuronal cells) antibody, and Hoechst 33342. Moreover, a fluorescent tracer (Fluorogold) was also injected into superior colliculi of the mice to label retinal ganglion cells. Results: Double positive staining of BrdU and NeuN antigen were detected in some cells in retinal ganglion cell layer of MEK1(E) transgenic mice at all the ages, 2 to 6 weeks, but not in that of wild type littermates. Some of the double labeled cells were also retrogradely labeled with Fluorogold. Furthermore, no BrdU positive cell was observed in the photoreceptor cell layer of either MEK1(E) transgenic mice or wild type mice. Conclusions: Retinal ganglion cells in MEK1(E) were able to continue to proliferate in responce to the enlargement of the eyeball up to the age of 6 weeks that we examined so far. This study also demonstrated that retinal ganglion cells were not only able to proliferate but also to differentiate to make the connection with the superior colliculi in the big eye transgenic mice at the later age. Therefore, we believe that an unknown factor in MEK1(E) transgenic mice induces the proliferation of the ganglion cells, since retinal ganglion cells in normal mice stop proliferation and differentiation at the age of two weeks. To further elucidate the mechanism for controlling the proliferation and differentiation of retinal ganglion cells and to identify this novel factor may provide us an alternative method to prevent the loss of ganglion cells in disease like glaucoma.

Keywords: ganglion cells • gene transfer/gene therapy • proliferation 
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